What If Alzheimer’s Can’t Be Cured?

This post may share a bit of ground with my last one (February 7th), but sometimes a little repetition is necessary.

The latest issue of JAMA Neurology is out (sorry folks, pay wall) with a study looking at “white matter hyperintensities” (WMH) in people’s brains. They have discovered a significant correlation between the amount of WMH and a diagnosis of Alzheimer’s Disease.

White matter hyperintensities are signs of small blood vessel disease in the brain that are seen on PET scans (positron emission tomography). While there has been inconsistent correlation to date between illness and amounts of amyloid in the brain, these cerebrovascular changes seem to be a better predictor of cognitive disability.

Let’s step WAY back for a moment. I am not as knowledgeable as the specialists on the details of brain pathology, but there are some basic considerations that keep popping out, that seem rather obvious to less sophisticated sorts like myself. Allow me to count them off on the fingers of my left hand, thus utilizing my right brain on this issue for a moment:

First, Alzheimer’s is not new. It was described by Dr. Alois Alzheimer over a century ago in a middle-aged woman, and no doubt has been around much longer than that. The population has skyrocketed in recent decades for three reasons: (1) better life expectancy, (2) more aging “Baby Boomers”, and (3) we are assigning the label to more people, as our testing becomes more sophisticated.

Second, we have found no easy answers to date–no clear causative factor(s) or effective treatments. And while younger people can develop Alzheimer’s, it is still by and large a condition of aging, and most people do not appear to have strong genetic factors in play.

Third, as I mentioned last time, there are many studies showing that “what’s good for the heart is good for the brain”, whether it be exercise, control of blood pressure, healthy diet, or avoidance of smoking.

Fourth, people with recurrent, clinically obvious strokes often develop dementia, so it makes sense that multiple tiny vascular lesions could also cause cognitive loss in a slower, more subtle manner.

Fifth, many people with amyloid plaques and tangles seen throughout their brains on autopsy never show evidence of dementia during their lives, suggesting that this hotbed of research may be less the cause and more the result of other changes. (There is a newer line of research looking at amyloid production within cells as a possible better avenue of investigation, but it still begs the question of what starts the whole process.)

So why does Alzheimer’s target certain areas of the brain most often? Maybe that’s where the vascular system is most susceptible to disruption. I don’t know if that’s true, but I am not sure anyone can fully explain why their proposed causative mechanisms might be targeting certain areas more than others.

I hate to be overly simplistic about this subject, but I was taught a principle in medical school called Occam’s Razor. Sir William of Ockham used this philosophy in the 14th century to discuss God and miracles, but it has since been co-opted by science, from Newton to the medical community. It means: Look for the simplest and most powerful answer to a problem, rather than introducing multiple factors that unnecessarily complicate a situation.

So at the risk of causing a few strokes among the research community, here’s a rather “naive” question: Is it possible that Alzheimer’s is the result of processes triggered by progressive vascular disease, as a consequence of aging, and that curing Alzheimer’s is difficult because we can neither cure aging nor the eventual deterioration of our cardiovascular apparatus?

And if that is the case, will there ever be a pill that can significantly reverse the process once these vascular changes take hold?

If these are valid questions, it would make our approach to prevention incredibly straightforward (healthy living and controlling risk factors) and also free up a lot of dollars to shift from dead-end avenues of research to improved systems of care for people living with cognitive disabilities.

Dangerous ideas, I know. A lot of people’s careers are hinging on all of this not being true. But maybe it’s time we confronted these questions more openly. It may be simpler than we would like to think.

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About Dr. Al Power, ChangingAging Contributor

Al Power is a geriatrician, author, musician, and an international educator on transformational models of care for older adults, particularly those living with changing cognitive abilities. You can follow his speaking schedule at http://www.alpower.net/gallenpower_schedule.htm

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Comments

Alzheimer’s disease involves changes in the brain, typically separation of different functions within its natural order. Hypothetically speaking, if this same separation decreases the electric wavelength of the brain, thus decreasing it’s connectivity, could there be some type of electronic stimulation that could repair the functioning?

I am currently an Aging 200 student at the Erickson School of Aging. I found this post to be very interesting because we covered the topic of dementia previously. I know that Alzheimer’s is a form of dementia. In my studies I found that a possible cause of dementia could be a result of high blood pressure and it was concluded that white matter hyperintensities cause increase stroke. These correlate because high blood pressure can cause strokes. I find Occam’s Razor philosophy to be very interesting and true. Sometimes we tend to overcomplicate things and think that there must be multiple causes for something as stated above. With the exceptions of younger people being diagnosed with the disease, most people that are diagnosed with Alzheimer’s are typically older. With that said, I agree with the statement that perhaps it is just a result of people aging. I personally find Alzheimer’s to be a very scary and serious disease but I feel that it really is just a part of aging.

I think we need to think even bigger than this. Vascular disease of any sort is bad for the brain, but the more we study the more we find out that it’s not just vascular disease but also changes in endocrine function (insulin, late life diabetes), our moods (depression and stress), our education, our social connectivity, and so forth. We need to be thinking of brain and body ecosystems!

The Ockam’s Razor principle is quite relevant. I remember reading about a study of Alzheimer’s disease in cloistered nuns. When a nun died, a brain autopsy would be performed. Amyloid plaque was often found and was present in the brain of one very old nun renowned for her remarkable, life-long cognitive abilities. Researchers came up with the concept of “cognitive reserve” to explain the unexpected result. It seems like quite a stretch. I think that Sir William of Ockam would object.

So if Alheimer’s and dementia are caused by mini-strokes and other vascular changes within the brain and that the drug companies are not going to be able to find a magic pill to cure it, could we not invest in the care of the currently demented and find better ways to involve them and keep them healthy? I currently work on a geri-psych acute care unit. We are always full and the diagnosis of preference is dementia with behavioral dyscontrol. These older people usually reside at nursing homes which are crowded and understaffed. There are few activities or ways to interact with other people. The residents slip farther and farther away from us. Maybe the focus should change from trying to cure it to trying to care for it and making the lives of those who suffer with it better?

I completely agree Al. I wish we could take even a fraction of the money given to research for a (possibly dead-end) cure and spend it instead on dealing with the fallout: supporting people who, for whatever reason, are dealing with a cognitive disability.

Here are some random thoughts.

At the very least, I would like to see EVERY person who is suspected of having cognitive loss being tested first for strokes. Automatic testing; do not pass GO. I know this sounds simplistic, but I’m not a doctor so I don’t even know the process of testing, but it seems very counterproductive, even knowing what we know now, to give someone a memory test, a diagnosis of Alzheimer’s, and send them home with a prescription, when all the while they may have a vascular condition that is only going to continue to make matters worse and probably, eventually, kill them.

I’m speaking from experience. My mother had vascular dementia that went undiagnosed and was ignored by her doctor. She had mild cognitive loss until a major and final stroke landed her in memory care, paralyzed. If the signs of minor strokes had not been ignored, things could have turned out much differently.

In fact, if “Alzheimer’s” becomes associated with and known as a heart condition, perhaps some of the stigma will diminish as well, and we can begin to take a more rehabilitative approach.

Thank you, Dr. Al–this is a very powerful and thought-provoking piece. And I’m always glad to hear someone remind us that the presence of amyloid plaques in the brain does not necessarily mean that one will develop dementia. This is not well known, given the focus of so much research on amyloid, and given the new PET scan that identifies amyloid plaques.

I agree that prevention is key. I write about some lesser-known risk factors, such as sleep apnea and pre-diabetes, in the appendices to my book “Inside the Dementia Epidemic: A Daughter’s Memoir.”